Nhibition on HepG2 cells, this appears to be the highest concentration ever to become reported for Uro-A anticancer activity in vitro and also greater than the previously reported plasma concentration (0.0245 ) of Uro-A glucuronide (38). Added caution ought to, for that reason, be taken in extrapolating in vitro effect into what occurs in vivo. UroB (15 ), on the other hand, inhibited the proliferation of HCC and induced a significant cell cycle arrest in the G0 /G1 phase in HepG2 cell and in the S phase in Bel7402 cells. UroB treatment also induced apoptosis, which can be LTE4 web evident in the decreased protein expression of Bcl-2. In vivo, Uro-B (40 mg/kg) suppressed tumor development in a xenograft mice model (one hundred). Uro-B’s antiproliferative prospective in each in vivo and in vitro is connected with an increase in phosphorylation of -catenin, blocking its translocation from the nucleus towards the cytoplasm and resulted in the inactivation of Wnt/-catenin signaling (61, 100).COLON CANCERColorectal cancer is a top bring about of death globally, affecting both genders in equal proportion. It can be ranked third and fourth with regards to cancer’s commonality and lead to of death, MAO-B custom synthesis respectively (101, 102). It slowly starts as a polyp within the interior lining of the rectal area in the colon. If left untreated, it metamorphoses into a cancer cell using the capacity to become metastasized to other areas in the body. The consumption of high-calorie meals, which include animal fat, can predispose a single to colon cancer (103).HEPATOCELLULAR CARCINOMAHepatocellular carcinoma (HCC) ranked sixth amongst all cancer types and second amongst cancer-causing death. In 2012, about 780,000 hepatocellular carcinoma instances were reportedlyFrontiers in Nutrition | www.frontiersin.orgJune 2021 | Volume 8 | ArticleAl-Harbi et al.Urolithins in Cancer PreventionIn colorectal cancer cell lines, urolithins exert their anticancer activity mainly by means of the promotion of apoptosis and cell cycle arrest (37, 48, 51, 52). In HT-29 colon cancer cell line, Uro-A (30 ml-1 ) and Uro-B (30 ml-1 ) mediate their antitumor potentials by means of apoptosis induction by activating caspase 3. These metabolites caused the upregulation in the expression of p21 protein and G2 /M phase arrest of the cell cycle (48). In Caco2 colon cancer cell lines, Uro-A in addition to Iso Uro-A, and within a time and dose-dependent manner (5000 , 248 h) triggered cell cycle arrest at each the S and G2 /M phases (37, 52) as well as the S phase by Uro-B, Uro-C, and Uro-D (52). Uro-A, UroC, and Uro-D also arrested cell cycle progression in the S-phase in SW480 and HT29 colon cancer cells (52). The anticancer potentials of urolithins may be as a consequence of the number of functional groups in their chemical structure, the effects of ionization on their stability, and the ionic charges in their microenvironment (51). These benefits indicate that the anticancer effects in the urolithins are cell-dependent. Autophagy is amongst the hallmarks of cancer. It truly is also a physiological response from the cell in which cellular organelles like the ribosomes and mitochondria are broken down inside the lysosomes. The catabolite obtained from the breakdown product is recycled and made use of for other metabolic processes and as a source of energy for the cell (104). Autophagy plays a critical role in colon cancer progression (105). At an early stage, autophagy inhibits tumor invasion and metastasis though advertising metastasis and survival at a later stage (63). Uro-A (15 ) and (30 ) concentrations resulted in th.
